Compensation versus deterioration across functional networks in amnestic mild cognitive impairment subtypes

Functional connectivity studies to detect neurophysiological correlates of amnestic mild cognitive impairment (aMCI), a prodromal stage of Alzheimer’s disease, have generated contradictory results in terms of compensation and deterioration, as most of the studies did not distinguish between the diff...

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Bibliographic Details
Authors: Varela-López, Benxamín; Zurrón Ocio, Montserrat; Lindín Novo, Mónica; Díaz Fernández, Fernando; Galdo Álvarez, Santiago
Format: Article
Publication date:2024
Country:España
Institution:Universidad de Santiago de Compostela (USC)
Repository:Minerva. Repositorio Institucional de la Universidad de Santiago de Compostela
Language:English
OAI Identifier:oai:minerva.usc.gal:10347/38994
Online Access:https://hdl.handle.net/10347/38994
Access Level:Open access
Keyword:Resting-state functional magnetic resonance imaging
Amnestic MCI
Amnestic MCI subtypes
Default mode network
Fronto-parietal control network
Description
Summary:Functional connectivity studies to detect neurophysiological correlates of amnestic mild cognitive impairment (aMCI), a prodromal stage of Alzheimer’s disease, have generated contradictory results in terms of compensation and deterioration, as most of the studies did not distinguish between the different aMCI subtypes: single-domain aMCI (sd-aMCI) and multiple-domain aMCI (md-aMCI). The present study aimed to characterize the neurophysiological correlates of aMCI subtypes by using resting-state functional magnetic resonance imaging. The study included sd-aMCI (n = 29), md-aMCI (n = 26), and control (n = 30) participants. The data were subjected to independent component analysis (ICA) to explore the default mode network (DMN) and the fronto-parietal control network (FPCN). Additionally, seed-based and moderation analyses were conducted to investigate the connectivity of the medial temporal lobe and functional networks. aMCI subtypes presented differences in functional connectivity relative to the control group: sd-aMCI participants displayed increased FPCN connectivity and reduced connectivity between the posterior parahippocampal gyrus (PHG) and medial structures; md-aMCI participants exhibited lower FPCN connectivity, higher anterior PHG connectivity with frontal structures and lower posterior PHG connectivity with central-parietal and temporo-occipital areas. Additionally, md-aMCI participants showed higher posterior PHG connectivity with structures of the DMN than both control and sd-aMCI participants, potentially indicating more severe cognitive deficits. The results showed gradual and qualitative neurofunctional differences between the aMCI subgroups, suggesting the existence of compensatory (sd-aMCI) and deterioration (mdaMCI) mechanisms in functional networks, mainly originated in the DMN. The findings support consideration of the subgroups as different stages of MCI within the Alzheimer disease continuum.